# PSORIASIS:  ITS GENOTYPE AND PATHOGENESIS:  MODEL SYSTEM

> **NIH NIH R01** · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · 1988 · $42,032

## Abstract

The broad objective remains:  The etiology of psoriasis.  The basic
hypothesis to be tested states that because baseline epidermal
proliferation is altered in skin of patients with psoriasis, there is a
cellular based message system within the skin that permits/causes the
altered epidermal proliferation.  The major specific aims are to define
this cellular component.  First, is the abnormal cellular component
causative to the epidermal hyperproliferation of psoriasis within the
epidermis (epidermal cells or Langerhans cells), the dermis (fibroblasts,
endothelial cells, mast cells, or Ia+ cells), or are all components
necessary?  Second, does the abnormal but equal hyperproliferation of the
epidermis of skin grafts from involved and uninvolved sites of psoriasis to
nude mice graduallly correct with prolonged times of engraftment?  If
correction does occur, what are the cellular changes and parameters which
defined this phenomenon?

The methodology to approach the goal of defining those cellular components
important to the hyperproliferation of the epidermis of patients with
psoriasis involves an artificial dermis containing and supporting specific
cell types.  The artificial dermis will support the proliferation and
differentiation of various epidermal combinations, epidermal sheets or
epidermal cell suspensions, from normal and psoriatic subjects, when
transplanted to the nude mouse.  Epidermal sheets maintained on this
artificial dermis appear to be devoid of Langerhans cells. This artificial
dermis can also be impregnated with fibroblasts from normal and psoriatic
subjects.  Dermal fragments can be placed under this thin, but very porous,
membrane, and the effects of various dermal types on epidermal
proliferation/differentiation determined.

The read-out system includes those changes in epidermal proliferation and
morphologic changes in the stratum corneum secondary to experimental
manipulations, comparing normal with psoriatic.  Experimental manipulations
include defined cell type on or in the artificial dermis and the response
of these skin equivalents of defined cell types to proliferative stimuli.
Conclusions as to the cell/ tissue causative to hyperproliferation of the
epidermis of psoriasis will be based upon depletion and reconstitution
experiments, normal vs. psoriasis.

## Key facts

- **NIH application ID:** 3155168
- **Project number:** 3R01AR021405-09S1
- **Recipient organization:** UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH
- **SAM.gov UEI:** LL8GLEVH6MG3
- **Principal Investigator:** GERALD Gene KRUEGER
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $42,032
- **Award type:** 3
- **Project period:** 1978-09-30 → 1989-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3155168

## Citation

> US National Institutes of Health, RePORTER application 3155168, PSORIASIS:  ITS GENOTYPE AND PATHOGENESIS:  MODEL SYSTEM (3R01AR021405-09S1). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3155168. Licensed CC0.

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